Submitted to: American Dairy Science Association Abstracts
Publication Type: Abstract only
Publication Acceptance Date: 7/27/1998
Publication Date: N/A
Citation: Interpretive Summary:
Technical Abstract: Production of NO by phagocytic leukocytes is required for microbial killing and signal transduction; however, excessive production is cytotoxic. Because the immune system of the neonate is generally hyporesponsive relative to that of the adult, and fat-soluble vitamins are known modulators of immune function, this study evaluated the capacity of blood mononuclear leukocytes from calves to produce NO and the effects of dietary vitamins A and E on NO production. Milk replacer-fed calves, 0 through 5 wk of age, received orally 100 IU/d of vitamin E as d-alpha-tocop or d-alpha-tocopheryl acetate and 0, 1700 (NRC requirement), 34,000 or 68,000 IU/d of vitamin A as retinyl acetate. Cells from 1-wk-old es produced less (P=.02) NO than cells from older calves, a possible consequence of suppressive factors present in the circulation at birth or acquired through ingestion of colostrum (1 L) fed within 6 h after birth. In general, calf leukocytes produced greater (P=.0001) amounts NO than adult leukocytes, which may be characteristic of the neonatal immune system. Cells from calves fed tocopherol produced less (P=.03) NO than those from calves fed tocopheryl acetate, regardless of level of vitamin A supplementation. Nitric oxide production by cells from calves fed tocopherol with 1700 or 34,000 IU/d of vitamin A was less (P less than .05) than NO production by cells from calves fed 0 or 68,000 IU/d of vitamin A and was not different (P more than .05) from amounts produced by adult cells. In conclusion, dietary vitamins A and E altered the capacity of calf mononuclear leukocytes to produce NO and suggests that these vitamins influence maturation of this aspect of the neonatal immune system.